Diagnostic and clinical manifestations Hepatic disorders Pancreatic disorders The nursing processes Functions of the liver It receives nutrientsrich blood from GIT It stores transforms these nutrients into chemicals to be used by the body ID: 629996
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Hepatic and Biliary dysfunction
Diagnostic and clinical manifestations
Hepatic disorders
Pancreatic disorders
The nursing processesSlide2
Functions of the liver
It receives nutrients-rich blood from GIT
It stores, transforms these nutrients into chemicals to be used by the body
Regulates glucose and protein metabolism
Manufactures and secretes bile for the digestion of fat
Removes waste products and secretes them into bile
The bile produced is stored in the gallbladder
Ammonia conversion: as a result of gluconeogenesis
Vitamins & iron storage
Bile formation
Drug metabolism Slide3
Anatomy & location
Behinds the ribs, in the upper portion of the abdominal cavity
Weighs 1200-1800 g
Divided into 4 lobes, separated by a thin layer of connective tissues; dividing the liver into small functional units, lobules
80% of blood supply comes from portal vein; the remainder from hepatic artery –rich in Oxygen
hepatic capillaries—sinusoids of liver—venules—composing the central vein—join to form the hepatic vein
Phagocytic cells, Kuffer cells are present in the liver Slide4
Anatomy & location
Canaliculi receives bile from hepatocytes—to a larger bile duct—to form the hepatic duct.
Hepatic duct joins the cystic duct from gallbladder to form the common bile duct—that empties into small intestine
Sphincter of Oddi, in the duodenum, control the flow of bile Slide5
Bile formation
Secreted by hepatocytes
Composed of water & electrolytes, lecthin, fatty acids, cholesterol, bilirubin.
Bile is synthesized from cholesterol after conjugation with amino acids (taurine& glycine)----required for emulsification of fats
Bilirubin is derived from moglobin then, conjugated which become more soluble ,
The conjugated bilirubin is secreted by hepatocytes and carried out in bile into duodenum.
In small intestine, it is converted into urobilinogen –excreted by feces or some is reabsorbed into portal circulation , some enter the systemic circulation and by kidneys.
Bilirubin increased in blood; in liver disease, gall bladder disese, destruction of RBCsSlide6
Hepatic dysfunction
Diagnostic evaluation
Liver function test
70% of parenchyma may be damaged before abnormal findings appear
Function is measured as serum enzymes:
Aminotransferase; alkaline phosphate; lactic dehydrogenase---released by liver cells damage --liver injury
Serum proteins: albumin & globulins, ammonia---liver impairment
Clotting factors and lipids; prothrombin time---liver cells damage
Bilirubin: liver and biliary tract disease, JaundiceSlide7
Diagnostic evaluation
Liver biopsy: Table 39-1, P 1290.
Obtain a sample of liver tissue via needle aspiration
Indications: diffuse disorders of the parenchyma
Major complications: bleeding, bile peritonitis---obtain coagulation studies before biopsy
Liver biopsy can be performed:
Percutaneously under ultrasound guidance
If ascites or coagulation abnormalities; other techniques are preferred
Transvenously through right internal jugular vein-to-right-hepatic vein under fluroscopic control
Other diagnostic tests: CT; MRI
Laboroscopy: insertion of fiberobtic endoscope via small abdominal incision to examine liver and pelvic structure; To obtain biopsy Slide8
Manifestation of hepatic dysfunction
Hepatic dysfunction results from primary liver disease, or
Indirectly: obstruction of bile flow; derangement of hepatic circulation
Can be acute or chronic; chronic is more common—chronic:
Liver cirrhosis—40% of deaths associate alcohol use
Uncommon, compensated and subclinical Cirrhoses ; often goes undetected
Causes of hepatocellular dysfunction: infectious agents, anoxia, metabolic disorder, nutritional deficiencies-alcohol related
Parenchymal damage: Noxious agents—liver cells replace glycogen with lipids—producing fatty infiltration—cell death or necrosis
Manifestations: jaundice, portal hyertension, ascites and varices, nutritional deficiencies and hepatic encephalopathy. Slide9
Most common clinical manifestations
Jaundice
Jaundice: abnormal elevation of bilirubin (exceeds 2.5 mg/dL)
Body tissues, including skin & sclerae, become tinged or greenish-yellow
Increased serum bilirubin may result from impairment of hepatic uptake, conjugation, excretion of bilirubin into biliary system
There are different types of jaundice:
Hemolytic Jaundice:
An increased destruction of the red blood cells—the liver can not excrete
Occurs in hemolytic disorders; transfusion reaction
The bilirubin ,in blood, is unconjugated or free
Fecal & urine urobilinogen are increased; urine is free from bilirubin
May have no symptoms, however, if exceeds 20-25 mg/dL---predispose brainstem damage; prolonged mild jaundice-- gallbladder stone; severe jaundiceSlide10
Most common clinical manifestations
Jaundice
Obstructive Jaundice:
Results from extra-hepatic obstruction due to gallbladder enlargement
Intra-hepatic obstruction: pressure on bile ducts within the liver; by inflammatory swelling of the liver or from
Stasis and inspissation (thickening) of bile within canaliculi-obstruction—after ingestion of medications: Phenothiazines, antithyroid, Sulfonylurea, tricyclic antidepressant…
In obstruction—bile can not flow into intestines—backed up in the liver---reabsorbed into blood—staining skin, mucous membrane, sclerae; stool become clay colored;excreted in the urine—becomes orange and foamy
Skin—severely itching requires soothing bath
Dyspepsia and intolerance to fatty foods
Serum bilirubin and alkaline phosphate are elevated Slide11
Most common clinical manifestations
Hepatocellular Jaundice
Damaged liver cells are unable to clear bilirubin from blood
Causes of damage: hepatitis viruses, medications, chemical toxins, alcohol
Cirrhosis of liver is a form of hepatocellular disease that produces jaundice; associate excessive alcohol use
Patients may experience mild or severe illness
Associated manifestations: loss of appetite, nausea, fatigue, possible weight loss
Serum bilirubin and urine urobilinogen may be elevated
If the cause is infection, patients may report headache and fever
May be completely reversible depending on the cause and extent of damage Slide12
Most common clinical manifestations
Hereditary hyperbilirubinemia
Results from several inherited disorders, Gilbert’s syndrome---increased un-conjugated serum bilirubin
Liver histology and function are normal
No hemolysisSlide13
Most common clinical manifestations
Portal Hypertension
Increased pressure in the portal venous system
Associates damaged liver that causes obstruction of blood flow
It associates hepatic cirrhosis; although occurs with non-cirrhotic liver
Manifestations: splenomegaly
Consequences: ascites and varicesSlide14
Ascites
Contributing factors:
Damaged liver—portal hypertension—increased capillary pressure & obstruction of venous blood flow
Vasodilation in the splanchnic circulation
Failure of the liver to metabolize Aldosterone—Na & water retention with:
Increased intravascular fluid volume
Increased lymphatic flow
Decreased synthesis of albumin
All contribute to movement of intravascular fluid into peritoneal space
Fluid in the peritoneal space—further retention; Na & water retension
Albumin-rich fluid moves into peritoneal space; 15 LSlide15
Ascites
assessment and clinical manifestations
Flank bulges with supine position
Percussion dullness and fluid shifting
Measure abdominal girth and weight daily to assess progress
Manifestations:
Increased abdominal girth
Shortness of breath; patients feel uncomfortable
Striae & distended vein may be visible
Fluid & electrolytes imbalances Slide16
Ascites
nursing and medical management
Dietary modifications: negative sodium balance to reduce retention
Avoid salty foods; low-sodium diets (2g sodium) is recommended
Substitute salts with lemon juice
Avoid substitutes that cause Ammonia;
Avoid substitutes that contain K if the patient has renal impairment
May reduce Na intake to 500 mg
If no responses with Na restriction; diureticsSlide17
Ascites
nursing and medical management
Diuretics:
Sodium restriction + diuretics are successful in 90%
First line: Spironolactone (Aldactone)
Is an aldosterone blocking agent
For ascites from cirrhosis
Preserves K
Furosemide (Lasix); may be added
Long-term use may induce hyopnatremiaSlide18
Ascites
nursing and medical management
Diuretics:
Ammonium chloride & Acetazolamide (Diamox) may precipitate hepatic coma—contraindicated
Daily weight loss should not exceed 1-2Kg in patient with ascites and edema; 0.5-0.75 in patients without edema
No fluid restriction unless serum Na is very low
Complications of diuretics:
Fluid & electrolytes disturbances;
Encephalopathy from dehydration and hypovolemia;
Impaired cerebral functioning when K is very low and serum ammonia increased
Slide19
Ascites
nursing and medical management
Bed rest:
Upright posture—activation of renin-angiotensin-aldosterone system & sympathetic nervous system—reduced glomerular filtration & Na excretion—decreased response to loop diuretics
Bed rest is useful for those refractory to diuretics Slide20
Ascites
nursing and medical management
Paracentesis: removal of fluid from peritoneal cavity via a puncture/small incision in the abdominal wall
Ultrasound guidance may be indicated in patients with abnormalities: coagulation, adhesions
Is currently performed for diagnostic purposes; in massive ascites—refractory to nutritional and diuretic therapy
Ascitic fluid for: cell count, albumin and proteins, culture
Removal of 5-6 liters is a safe procedure + IV infusion of salt-poor Albumin/other colloids is a standard management approach
Albumin infusion helps to correct decrease in effective arterial blood volume
Read guidelines for assisting patients with paracentesis (P 1126, Chart 39-3). Transjugular intrahepatic portosystemic shunt. Slide21
Nursing management
home & community based care
For hospitalized: Assessment of fluid status; intake & output; abdominal girth; daily Wt.
Assessment of electrolytes balance: serum ammonia, electrolytes, indications of encephalopathy
Teaching self-care:
Avoid alcohol intake
Adhere to low sodium diet, medications
Skin care and the need for daily Wt.
To report sign & symptoms of complications
Assess home environment & resources available
Assessment of adherence to treatment plan
Keep up with appointments Slide22
Esophageal Varices
Occur In majority of patients with cirrhosis
Are varicosities develop from elevated pressure in veins that drain into portal system
Are prone to rupture—source of massive hemorrhage from upper GI tract and the rectum
Coagulation abnormalities increase bleeding & blood loss
Are the significant source of bleeding, In liver cirrhosis
Varices once form, they increase in size and bleed
First bleeding has a mortality rate of 30-50%Slide23
Esophageal varices
pathophysiology
Are dilated tortuous veins in submucosa of lower esophagus
Damaged liver—obstruction of portal venous circulation—portal hypertension
Because of obstruction—venous blood from intestinal & spleen tract seeks outlet through collateral circulation to right atrium—tortuous & fragile—rupture & bleed
Are life-threatening—hemorrhagic shock—leading to--decreased hepatic, cerebral, renal perfusion
Bleeding in GI—increased nitrogen load & serum ammonia—increased risk of encephalopathy
Contributing factors to hemorrhage: muscular exertion-heavy lifting; straining, sneezing-vomiting-coughing; irritating foods, reflux of stomach content (Alcohol); Salicylates Slide24
Esophageal varices
Diagnoses and assessment
Signs of bleeding: hematemesis, melena, deterioration in mental & physical states; history of alcohol abuse
Signs of shock: cool clammy skin, hypotension, tachycardia
Endoscopy, barium swallow, CT, angiography
In patients with cirrhosis—screening endoscopy every 2 years to identify & treat large varices
Careful monitoring can detect early signs of cardiac dysrhythmias, perforations, hemorrhage
After examinations:
Fluid are not permitted until gag reflex returns
Lozenges & gargles to relive throat discomfort if physiologically permitted
No oral intake in active bleedingSlide25
Portal hypertension measurement
Indications: dilated abdominal veins, hemorrhoids, splenomegaly,ascites
Indirect measurement of hepatic vein pressure is the most common
Insertion of a catheter with a balloon into antecubital or femoral vein
Then advanced under fluoroscopy to a hepatic vein
Fluid is infused to inflate the balloon
A wedged pressure is obtained by occluding blood flow
Pressure in the un-occluded vessel is obtained
Direct measurement: Laparotomy—needle in spleen—manometer
More than 20 ml saline is abnormal
Blood tests: liver function tests—serum aminotransferase, bilirubin, alkaline phosphate, serum proteins Slide26
Esophageal varices
Nursing and medical management
Bleeding from EV requires aggressive medical care, expert nursing, ICU for frequent vital signs measurement
Monitoring for indicators of hemorrhagic shock
Central venous pressure to evalute blood volume and arterial line
Oxygen to prevent hypoxia & maintain adequate blood oxygenation
IV fluids, electrolytes & expanders to restore blood volume
Transfusion of blood components may be required
Caution: overhydration—raise portal hypertension—increases bleeding
Indwelling urinary catheter to monitor urine output
Nonsurgical management minimizes risk of mortality; and because of poor physical condition related to severe liver dysfunction Slide27
Esophageal varices
pharmacologic therapy
In active bleeding; Vasopressin (Pitressin) produces constriction of splanchnic arterial bed—reducing blood flow in the portal system & decreases portal hypertension
Effectiveness of vasopressin: vital signs and blood-free gastric aspirate
Has anti-diuretic effect and hyponatremia may develop: monitor intake & output, electrolytes
Contraindicated in CADs; can be used with nitroglycerin
Side effects of vasopressin: ischemia & dysrhythmias; add nitroglycerin
Somatostatin & Octreotide (Sandostatin) effective in decreasing bleeding; has no vasconstrictive effect; have selective effects
Other medications: propranolol & nadolol, Beta blocker agents—decrease portal pressure—prevent bleeding episodes; Beta-blockers should not be used in acute hemorrage; just as prophylaxis
Nitrates (isordil): lower portal pressure by venodilation. Slide28
Esophageal varices
balloon tamponade
To control hemorrhage; exertion of pressure on the cardia by a double-balloon tamponade
Sengstaken-Blakemore tube has 4 openings: gastric aspiration, esophageal aspiration, balloon inflation (gastric & esophagus)
In stomach, Inflated with 100-200 ml of air; then pulled & traction applied; pressure in esophageal & gastric balloons is 25 – 40mm HG
Continuous low suctioning with hourly irrigation to detect bleeding
Irrigastion; and Pressure measurement every 2-4 hours to prevent esophageal injury & under-inflation
After several hours of no bleeding, can be deflated safely; if still no bleeding can be removed
Danger: displacement, inflation into oropharynx, rupture—pulmonary aspiration—ET tube to protect from aspiration ; necrosis—long periodSlide29
Esophageal varices
other medical management
Endoscopic sclerotherapy:
Injection of sclerosing agent into esophageal varices via fiberobtic endoscope—to promote thrombosis
After treatment observe for bleeding, perforation of esophagus, esophageal stricture, aspiration pneumonia
Antacids, Cimetidine or Pantoprazole (Protonix), a proton pump inhibitor may be given to counteract the sclerosing agent
Surgical management:
Variceal banding
Portal systemic shunt
Read management modalities (Table 39-2 P. 1134)Slide30
Esophageal varices
nursing actions
Continuous monitoring of physical, emotional & mental status
Assess vital signs & nutritional status
GI bleeding-elevated serum ammonia causing drowsiness to profound coma
Parenteral nutrition if complete rest of esophagus is indicated
Gastric suctioning to prevent straining & vomiting
Frequent oral hygiene & moist sponge to the lips to prevent thirst feeling
blood transfusions & Vit K therapy
Quiet environment & reassurance to relieve anxiety
Delirium secondary to alcohol withdrawal may occur; anxiety
Provide support & explanation about medical therapies Slide31
Hepatic encephalopathy and coma
Porto-systemic encephalopathy is a life-threatening complication occurs with liver failure
Is neuropsychiatric manifestation of hepatic failure associates portal hypertension or shunting of blood from portal into systemic circulation
Is a reversible metabolic form of encephalopathy
Can improve with recovery of liver function
Occurs in stages; (read Table 39-3, P 1132)Slide32
Hepatic encephalopathy
Pathophysiology
Occurs because
Inability of liver to detoxify toxic byproducts of metabolism
Shunting allows elements of portal blood to enter systemic circulation; collateral circulation
Ammonia is the major etiologic factor—enter the brain—increasing neuro-steroid synthesis; that stimulates gamma aminobutyric acid—causing depression of the CNS
Ammonia inhibits neurotransmission & synaptic regulations—producing sleep & behavior patterns that associate hepatic encephalopathySlide33
Hepatic encephalopathy
Pathophysiology
Major source of ammonia: enzymatic & bacterial digestion of dietary & blood proteins in GI
Other factors that increases ammonia are GI Bleeding; high protein diet; bacterial infection; uremia
With alkalosis / hypokalemia increased amount of ammonia is absorbed from GI.
Serum ammonia is decreased by:
Elimination of protein from the diet
Administration of antibiotics, Neomycin sulfate; decreases intestinal bacteria that covert urea to ammonia Slide34
Hepatic encephalopathy
assessment and diagnosis
EEG: generalized slowing, increased amplitude of brain wave
Early symptoms: minor mental changes and motor disturbances;
Confusion with altered mood & sleep pattern—tends to sleep during day with restlessness & insomnia at night
With progress, disorientation to time & place
Further progression: frank coma, Seizures
Other manifestations:
Asterixis: flapping tremor of hands; also hand writing becomes difficult, seen in stage 2,
Constructional apraxia: inability to reproduce a simple figure
Fetor hepaticus: fecal odor to the breath; is prevalent in extensive collateral circulation Slide35
Hepatic encephalopathy
medical management
Principle of management
Elimination of precipitating factors
Initiating ammonia-lowering therapy
Minimizing potential complications of cirrhosis & coma
Reversing the underlying liver disease
Lactulose: orally; or by nasogastric tube or enema if orally is not allowed
Reduces serum ammonia by promoting excretion of ammonia in stool
Monitor for watery diarrheal stool
Side effects: intestinal bloating & cramping
Can be diluted with fruit juice to mask sweet taste
Monitor for hypokalemia, dehydration
Other laxatives are not prescribed with lactulose intake Slide36
Hepatic encephalopathy
medical management
IV glucose to minimize protein breakdown
Vitamins to correct deficiencies, correction of electrolytes, K
Antibiotics: neomycin, Flagyl, Rifaximin to reduce ammonia forming bacteria
Additional principles of management
Assess mental status, daily handwriting
Daily intake & output, weight
Protein intake is moderately restricted—for comatose patients
Vital signs every 4 hours, serum ammonia daily
Assess potential sites of infection, peritoneum, lungs
Read page 1136 for further principles of management of encepahlopathySlide37
Hepatic encephalopathy
medical management
Moderate restriction of protein intake
Long-term restriction-less than 1 gm / Kg daily should be avoided
Vegetables or dairy proteins can be used; UP TO 12O Gms/day
Advised: Food high in proteins, meat, eggs, should be eliminated from the diet for short-term. (Read chart 39-5, P 1136).
Enteral feeding if encephalopathy persists
Monitor and correct electrolyte status; I & O
Discontinue Sedatives, Tranquilizers, analgesics
Flumazenil (Romazicon), a Benzodiazepine antagonist may be given to improve encephalopathy
Reduction of ammonia absorption by gastric suction, enema, antacidsSlide38
Hepatic encephalopathy
nursing management
Maintain safe environment to prevent injury, bleeding, infection
Prevent respiratory complications
Family support and reassurance
Teaching self care:
Watch for subtle signs of recurrent encephalopathy
Restriction of protein intake (0.8-1 gm/Kg daily), moderate protein-High caloric diet
Use of vegetable proteins
Use of lactulose to prevent constipationSlide39
Viral hepatitis
Is a systemic viral infection-necrosis & inflammation of liver cells produce a cluster of clinical, biochemical & cellular changes
Definitive types of hepatitis are A, B ,C,D,E
Is easily transmitted
Causes morbidity & prolonged loss of time from school or employment
Occurrence rate has been decreased because of A & B vaccines & public education Slide40
Hepatitis A Virus
HAV accounts for 20-25% of cases of clinical hepatitis
Caused by RNA virus; HAV
Is seen mainly in adult population
Transmitted through fecal-oral route-ingestion of food-liquid infected
More prevalent in overcrowding & poor sanitation places; as a result of poor hygiene
Virus is found in the stool of infected persons before symptoms onset & during the first few days of illness
Can be transmitted during sexual activity
Incubation period 2-6 weeks; M = 4 Weeks
Rarely progresses to acute liver necrosis / cirrhosis
No carrier state exists; the virus presents briefly in the serum Slide41
HAV
Assessment & diagnosis
Many Patients are anicteric (no Jaundice) & symptomless
If symptoms present: Resemble mild flulike of upper respiratory tract infection with Low-grade fever
Severe anorexia—an early symptom—result from release of toxins from the damaged liver or inability of the liver to detoxify abnormal products; Later; jaundice & dark urine
indigestion with epigastric distress, nausea, heartburn, flatulence
A strong aversion to taste of cigarettes
Symptoms tend to clear as jaundice reach the peak, 10-days after appearance
Liver & spleen enlargement; hepatitis A antigen in the stool
HAV antibodies in the serum Slide42
HAV
Prevention
Scrupulous hand washing, safe water supplies, proper control of sewage disposal
Vaccination: 2 times for adult, 18-year or older with 6-12 months apart
3 times for children with 1-month & 6-12 months apart
For those with no vaccination; IM of globulin during incubation period
Medical management:
Bed rest; acceptable & nutritious diet
In anorexia: Frequent small feedings supplemented by IV fluids with glucose
Optimal food & fluid intake to prevent weight loss & to speed recovery
Gradual progressive ambulation may hasten recovery
Teach patient to: Avoid alcohol; Have proper hygiene; Seek care
Read charts: 39-7 and 39-8; P. 1141 Slide43
Hepatitis B virus
Transmitted through blood; percutaneous or permucosal routes
Or from carrier mother to their infants at time of birth
Found in blood, saliva, semen, vaginal secretions; has a long incubation period; replicates in the liver & remains in serum
Who contract HBV develop antibodies and recover within 6 months
10% progress to carrier or develop chronic hepatitis—hepatocellular injury & inflammation
In elderly may progress to severe cell necrosis or hepatic failure; because of alteration in the immune system
So, factors that affect liver function should be eliminated; medications, alcohol
Risk Factors; read chart 39-9, P. 1141.Slide44
HBV
assessment & diagnosis
Symptoms similar to that of HAV; although are rare; much longer incubation period, 1-6 months
Arthralgia, rashes
Loss of appetite, dyspepsia, generalized aching , malaise & weakness
Jaundice with dark urine& light-colored stool may appear
Liver tender and enlarged; spleen is enlarged
Has different antigen: HBcAg; HBsAg, HBeAg, HBxAg
For each antibodies are developed: anti HBs, HBc, Hbe, HBx.
HBsAg appear in 90% ; if persists for more than 6 months; patient is a carrier Slide45
HBV
Prevention
General precaution to prevent transmission
Screening blood donors; Read preventing transmission, P. 1142.
Precautions related to healthcare providers
Immunization
Active immunization with Recombivax HB
for those at high risk: healthcare providers, hemodialysis patients, & those with hepatitis C
Has an effect for 5-10 years, booster doses for immunocompromised patients
Given IM in 3 doses; with 1 & 6 months apart, in the deltoid muscle
Passive immunity: HBIG, hepatis B immune globulin; for those exposed to HBV given within hours to few days Slide46
HBV
Medical management
Alpha-interferon: 5 million units daily or 10 million units 3 times a week for 16-24 weeks
Side effects: fever, chills, anorexia, nausea, fatigue
Delayed side effects: bone marrow depression, thyroid dysfunction, alopecia,; may necessitate reduction of the dose
Antiviral agents may be used: Lamivudine, Adefovir
Bed rest may be recommended until symptoms subsided;
Activity is restricted until liver enlargement & serum bilirubin are decreased
Maintain adequate nutrition; protein restriction may be required; if liver ability to metabolize proteins is impaired
In case of vomiting, hospitalization for fluid replacement Slide47
HBV
Nursing actions
Convalescence period: 3-4 months
Identify psychosocial responses
Teach and provide necessary steps in medical management
Read Table 39-4, P 1139 for other forms of Hepatitis
Slide48
Hepatic cirrhosis
Is a chronic disease in which liver tissues are replaced by diffuse fibrosis that disrupts structure & function of the liver
Types of cirrhosis:
Alcoholic cirrhosis: scar tissue surrounds portal area
Postnecrotic cirrhosis: there are broad bands of scar tissue, a result of acute viral hepatitis
Biliary cirrhosis: scarring around bile ducts, a result of chronic biliary obstruction Slide49
Hepatic cirrhosis
pathophysiology
Major causative factors: Alcohol consumption; nutritional deficiency; exposure to certain chemicals, carbon, arsenic, phosphorus
Alcoholic cirrhosis: episodes of liver cells necrosis—replaced by scar tissues—exceeds that of functioning liver tissue—re-generating liver tissue project from constricted areas giving hobnail appearance
Severity of symptoms characterizes cirrhosis as
Compensated: has vague symptoms, discovered accidently
Decompensated: results from failure of the liver to synthesize proteins, clotting factors, other substances; complications
Manifestations: Hepatic dysfunction manifestations; edema, GIT: distended abdominal BVs; vitamins deficiency & anemia; mental deterioration. READ TABLE 39-5 & CHART 39-11; P. 1147.Slide50
Hepatic cirrhosis
medical management
Depends on Symptoms
Antacids & antihistanie-2 to minimize GI bleeding
Vitamins and nutritional supplements promote healing
Diuretics for ascites; spironolactone to decrease ascites
Colchicine has anti-inflammatory effect may increase survival time
Some medications show antifibrotic effect, statins, diuretics, immunosuppressants
In ESLD, Herb milk thistle: has anti-inflammatory effect & antioxidant properties
Ursodeoxycholic acid for biliary cirrhosis to improve liver function Slide51
Hepatic cirrhosis
nursing actions
Read chart 39-12, P 1150-1157 for more details
Promoting rest:
To decrease demands on the liver & increases liver’s blood supply
Adjust position for respiratory efficiency, O2 therapy to prevent cell destruction;
Measures to prevent complications of immobility
Weight, and intake & output daily
Encourage gradual increase in activity once nutritional status improvesSlide52
Hepatic cirrhosis
nursing actions
Improving nutritional status:
In cirrhosis without edema, ascites or sign of hepatic coma; give a nutritious high protein diet supplemented by vitamins
In ascites, frequent small meals; consider patients preferences
In severe anorexia, enteral or parenteral feeding may be given
In patient with fatty stool (steatorrhea), give water-soluble vitamins: A, D & E
In impending coma decrease protein in the diet; if encephalopathy develops, restrict protein intake
Vegetable protein to meet the patient needs
Sodium restriction in ascitesSlide53
Hepatic cirrhosis
nursing actions
Providing skin care: because of subcutaneous edema, immobility, jaundice,
Frequent position changes
Avoid irritating soap & adhesive tape to prevent trauma
Lotion to sooth irritated skin, minimize scratching
Reducing risk of injury:
Prevent fall, padded side rails
Minimize agitation by orientation to time & place, explain all procedures
Minimize bleeding; electronic razor, soft-bristled toothbrush, pressure to all venipuncture